Progress in experimental research on pulsed electromagnetic field in the treatment of knee osteoarthritis_West China Medical Journal

Authors：

YANG Xiaotian ,  HE Chengqi

Rehabilitation Medicine Center, West China Hospital, Sichuan University; Rehabilitation Key Laboratory of Sichuan Province; Chengdu, Sichuan 610041, P. R. China;

Corresponding author：

HE Chengqi, Email: hxkfhcq@126.com

Keywords：

Osteoarthritis; Pulsed electromagnetic field; Rehabilitation treatment

DOI：

10.7507/1002-0179.201702221

Video：

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With the acceleration of the aging in the world and our society, osteoarthritis has become a health concern for patients and health workers. At present, its treatment mainly relies on drug treatment, surgical treatment and rehabilitation. As a safe, non-invasive and simple treatment, pulsed electromagnetic field (PEMF) therapy has been used in clinical treatment of osteoporosis, promoting fracture healing and improving symptoms of osteoarthritis. However, the mechanism of PEMF in the treatment of knee osteoarthritis is still unclear. This paper reviews the effects of PEMF on apoptosis, cytokines, cartilage and subchondral bone in knee osteoarthritis in animal experiments, and the changes of chondrocyte morphology and extracellular matrix in cell experiments, aiming to enable medical workers to better understand the status and development of PEMF in the treatment of knee osteoarthritis in basic experimental researches.

Citation： YANG Xiaotian, HE Chengqi. Progress in experimental research on pulsed electromagnetic field in the treatment of knee osteoarthritis. West China Medical Journal, 2018, 33(9): 1186-1190. doi: 10.7507/1002-0179.201702221 Copy

1.	Abramson SB, Attur M. Developments in the scientific understanding of osteoarthritis. Arthritis Res Ther, 2009, 11(3): 227.
2.	Lories RJ, Luyten FP. The bone-cartilage unit in osteoarthritis. Nat Rev Rheumatol, 2011, 7(1): 43-49.
3.	Fernandes L, Hagen KB, Bijlsma JW, et al. EULAR recommendations for the non-pharmacological core management of hip and knee osteoarthritis. Ann Rheum Dis, 2013, 72(7): 1125-1135.
4.	Hochberg MC, Altman RD, April KT, et al. American college of rheumatology 2012 recommendations for the use of nonpharmacologic and pharmacologic therapies in osteoarthritis of the hand, hip, and knee. Arthritis Care Res (Hoboken), 2012, 64(4): 465-474.
5.	Mcalindon TE, Bannuru RR, Sullivan MC, et al. OARSI guidelines for the non-surgical management of knee osteoarthritis. Osteoarthritis Cartilage, 2014, 22(3): 363-388.
6.	Liu H, Yang L, He H, et al. The hemorheological safety of pulsed electromagnetic fields in postmenopausal women with osteoporosis in southwest China: a randomized, placebo controlled clinical trial. Clin Hemorheol Microcirc, 2013, 55(3): 285-295.
7.	Liu HF, Yang L, He HC, et al. Pulsed electromagnetic fields on postmenopausal osteoporosis in Southwest China: a randomized, active-controlled clinical trial. Bioelectromagnetics, 2013, 34(4): 323-332.
8.	Chalidis B, Sachinis N, Assiotis A, et al. Stimulation of bone formation and fracture healing with pulsed electromagnetic fields: biologic responses and clinical implications. Int J Immunopathol Pharmacol, 2011, 24(1 Suppl 2): 17-20.
9.	Ryang We S, Koog YH, Jeong KI, et al. Effects of pulsed electromagnetic field on knee osteoarthritis: a systematic review. Rheumatology (Oxford), 2013, 52(5): 815-824.
10.	Li S, Yu B, Zhou D, et al. Electromagnetic fields for treating osteoarthritis. Cochrane Database Syst Rev, 2013(12): CD003523.
11.	Esposito E, Cuzzocrea S. TNF-alpha as a therapeutic target in inflammatory diseases, ischemia-reperfusion injury and trauma. Curr Med Chem, 2009, 16(24): 3152-3167.
12.	Riyazi N, Slagboom E, de Craen AJ, et al. Association of the risk of osteoarthritis with high innate production of interleukin-1beta and low innate production of interleukin-10 ex vivo, upon lipopolysaccharide stimulation. Arthritis Rheum, 2005, 52(5): 1443-1450.
13.	Larsson S, Englund M, Struglics A, et al. Interleukin-6 and tumor necrosis factor alpha in synovial fluid are associated with progression of radiographic knee osteoarthritis in subjects with previous meniscectomy. Osteoarthritis Cartilage, 2015, 23(11): 1906-1914.
14.	Ma CH, Lv Q, Yu YX, et al. Protective effects of tumor necrosis factor-α blockade by adalimumab on articular cartilage and subchondral bone in a rat model of osteoarthritis. Braz J Med Biol Res, 2015, 48(10): 863-870.
15.	Guo H, Luo Q, Zhang J, et al. Comparing different physical factors on serum TNF-α levels, chondrocyte apoptosis, caspase-3 and caspase-8 expression in osteoarthritis of the knee in rabbits. Joint Bone Spine, 2011, 78(6): 604-610.
16.	Daheshia M, Yao JQ. The interleukin 1 beta pathway in the pathogenesis of osteoarthritis. J Rheumatol, 2008, 35(12): 2306-2312.
17.	Ciombor DM, Aaron RK, Wang S, et al. Modification of osteoarthritis by pulsed electromagnetic field--a morphological study. Osteoarthritis Cartilage, 2003, 11(6): 455-462.
18.	Zhao W, Wang T, Luo Q, et al. Cartilage degeneration and excessive subchondral bone formation in spontaneous osteoarthritis involves altered TGF-β signaling. J Orthop Res, 2016, 34(5): 763-770.
19.	Zhai GJ, Dore J, Rahman P. TGF-beta signal transduction pathways and osteoarthritis. Rheumatol Int, 2015, 35(8): 1283-1292.
20.	Yang CC, Lin CY, Wang HS, et al. Matrix metalloproteases and tissue inhibitors of metalloproteinases in medial plica and pannus-like tissue contribute to knee osteoarthritis progression. PLoS One, 2013, 8(11): e79662.
21.	Settle S, Vickery L, Nemirovskiy O, et al. Cartilage degradation biomarkers predict efficacy of a novel, highly selective matrix metalloproteinase 13 inhibitor in a dog model of osteoarthritis: confirmation by multivariate analysis that modulation of type Ⅱ collagen and aggrecan degradation pepti. Arthritis Rheum, 2010, 62(10): 3006-3015.
22.	Zamli Z, Adams MA, Tarlton JF. Increased chondrocyte apoptosis is associated with progression of osteoarthritis in spontaneous Guinea pig models of the disease. Int J Mol Sci, 2013, 14(9): 17729-17743.
23.	Musumeci G, Castrogiovanni P, Trovato FM, et al. Biomarkers of chondrocyte apoptosis and autophagy in osteoarthritis. Int J Mol Sci, 2015, 16(9): 20560-20575.
24.	谢薇, 周君, 罗庆禄, 等. 脉冲电磁场对兔膝骨关节炎软骨细胞凋亡及凋亡调控蛋白的影响. 四川大学学报: 医学版, 2014(1): 107-110.
25.	Mankin HJ, Dorfman H, Lippiello L, et al. Biochemical and metabolic abnormalities in articular cartilage from osteo-arthritic human hips. Ⅱ. Correlation of morphology with biochemical and metabolic data. J Bone Joint Surg Am, 1971, 53(3): 523-537.
26.	Pritzker KP, Gay S, Jimenez SA, et al. Osteoarthritis cartilage histopathology: grading and staging. Osteoarthritis Cartilage, 2006, 14(1): 13-29.
27.	Carlson CS, Loeser RF, Purser CB, et al. Osteoarthritis in cynomolgus macaques. Ⅲ: Effects of age, gender, and subchondral bone thickness on the severity of disease. J Bone Miner Res, 1996, 11(9): 1209-1217.
28.	Pastoureau PC, Hunziker EB, Pelletier JP. Cartilage, bone and synovial histomorphometry in animal models of osteoarthritis. Osteoarthritis Cartilage, 2010, 18(Suppl 3): S106-S112.
29.	Laverty S, Girard CA, Williams JM, et al. The OARSI histopathology initiative - recommendations for histological assessments of osteoarthritis in the rabbit. Osteoarthritis Cartilage, 2010, 18(Suppl 3): S53-S65.
30.	Gerwin N, Bendele AM, Glasson S, et al. The OARSI histopathology initiative - recommendations for histological assessments of osteoarthritis in the rat. Osteoarthritis Cartilage, 2010, 18(Suppl 3): S24-S34.
31.	De Mattei M, Pasello M, Pellati A, et al. Effects of electromagnetic fields on proteoglycan metabolism of bovine articular cartilage explants. Connect Tissue Res, 2003, 44(3/4): 154-159.
32.	De Mattei M, Pellati A, Pasello M, et al. Effects of physical stimulation with electromagnetic field and insulin growth factor-Ⅰ treatment on proteoglycan synthesis of bovine articular cartilage. Osteoarthritis Cartilage, 2004, 12(10): 793-800.
33.	De Mattei M, Fini M, Setti S, et al. Proteoglycan synthesis in bovine articular cartilage explants exposed to different low-frequency low-energy pulsed electromagnetic fields. Osteoarthritis Cartilage, 2007, 15(2): 163-168.
34.	Fini M, Giavaresi G, Torricelli P, et al. Pulsed electromagnetic fields reduce knee osteoarthritic lesion progression in the aged Dunkin Hartley Guinea pig. J Orthop Res, 2005, 23(4): 899-908.
35.	Fini M, Torricelli P, Giavaresi G, et al. Effect of pulsed electromagnetic field stimulation on knee cartilage, subchondral and epyphiseal trabecular bone of aged Dunkin Hartley Guinea pigs. Biomed Pharmacother, 2008, 62(10): 709-715.
36.	Veronesi F, Torricelli P, Giavaresi G, et al. In vivo effect of two different pulsed electromagnetic field frequencies on osteoarthritis. J Orthop Res, 2014, 32(5): 677-685.
37.	Chiba K, Nango N, Kubota S, et al. Relationship between microstructure and degree of mineralization in subchondral bone of osteoarthritis: a synchrotron radiation μCT study. J Bone Miner Res, 2012, 27(7): 1511-1517.
38.	Hayami T, Pickarski M, Wesolowski GA, et al. The role of subchondral bone remodeling in osteoarthritis: reduction of cartilage degeneration and prevention of osteophyte formation by alendronate in the rat anterior cruciate ligament transection model. Arthritis Rheum, 2004, 50(4): 1193-1206.
39.	Kwan Tat S, Lajeunesse D, Pelletier JP, et al. Targeting subchondral bone for treating osteoarthritis: what is the evidence?. Best Pract Res Clin Rheumatol, 2010, 24(1): 51-70.
40.	Castañeda S, Roman-Blas JA, Largo R, et al. Subchondral bone as a key target for osteoarthritis treatment. Biochem Pharmacol, 2012, 83(3): 315-323.
41.	Jahns ME, Lou E, Durdle NG, et al. The effect of pulsed electromagnetic fields on chondrocyte morphology. Med Biol Eng Comput, 2007, 45(10): 917-925.
42.	Varani K, De Mattei M, Vincenzi F, et al. Characterization of adenosine receptors in bovine chondrocytes and fibroblast-like synoviocytes exposed to low frequency low energy pulsed electromagnetic fields. Osteoarthritis Cartilage, 2008, 16(3): 292-304.
43.	Schmidt-Rohlfing B, Silny J, Woodruff S, et al. Effects of pulsed and sinusoid electromagnetic fields on human chondrocytes cultivated in a collagen matrix. Rheumatol Int, 2008, 28(10): 971-977.
44.	Chang CH, Loo ST, Liu HL, et al. Can low frequency electromagnetic field help cartilage tissue engineering?. J Biomed Mater Res A, 2010, 92(3): 843-851.
45.	Chang SH, Hsiao YW, Lin HY. Low-frequency electromagnetic field exposure accelerates chondrocytic phenotype expression on chitosan substrate. Orthopedics, 2011, 34(1): 20.
46.	Sadoghi P, Leithner A, Dorotka R, et al. Effect of pulsed electromagnetic fields on the bioactivity of human osteoarthritic chondrocytes. Orthopedics, 2013, 36(3): e360-e365.

1. Abramson SB, Attur M. Developments in the scientific understanding of osteoarthritis. Arthritis Res Ther, 2009, 11(3): 227.
2. Lories RJ, Luyten FP. The bone-cartilage unit in osteoarthritis. Nat Rev Rheumatol, 2011, 7(1): 43-49.
3. Fernandes L, Hagen KB, Bijlsma JW, et al. EULAR recommendations for the non-pharmacological core management of hip and knee osteoarthritis. Ann Rheum Dis, 2013, 72(7): 1125-1135.
4. Hochberg MC, Altman RD, April KT, et al. American college of rheumatology 2012 recommendations for the use of nonpharmacologic and pharmacologic therapies in osteoarthritis of the hand, hip, and knee. Arthritis Care Res (Hoboken), 2012, 64(4): 465-474.
5. Mcalindon TE, Bannuru RR, Sullivan MC, et al. OARSI guidelines for the non-surgical management of knee osteoarthritis. Osteoarthritis Cartilage, 2014, 22(3): 363-388.
6. Liu H, Yang L, He H, et al. The hemorheological safety of pulsed electromagnetic fields in postmenopausal women with osteoporosis in southwest China: a randomized, placebo controlled clinical trial. Clin Hemorheol Microcirc, 2013, 55(3): 285-295.
7. Liu HF, Yang L, He HC, et al. Pulsed electromagnetic fields on postmenopausal osteoporosis in Southwest China: a randomized, active-controlled clinical trial. Bioelectromagnetics, 2013, 34(4): 323-332.
8. Chalidis B, Sachinis N, Assiotis A, et al. Stimulation of bone formation and fracture healing with pulsed electromagnetic fields: biologic responses and clinical implications. Int J Immunopathol Pharmacol, 2011, 24(1 Suppl 2): 17-20.
9. Ryang We S, Koog YH, Jeong KI, et al. Effects of pulsed electromagnetic field on knee osteoarthritis: a systematic review. Rheumatology (Oxford), 2013, 52(5): 815-824.
10. Li S, Yu B, Zhou D, et al. Electromagnetic fields for treating osteoarthritis. Cochrane Database Syst Rev, 2013(12): CD003523.
11. Esposito E, Cuzzocrea S. TNF-alpha as a therapeutic target in inflammatory diseases, ischemia-reperfusion injury and trauma. Curr Med Chem, 2009, 16(24): 3152-3167.
12. Riyazi N, Slagboom E, de Craen AJ, et al. Association of the risk of osteoarthritis with high innate production of interleukin-1beta and low innate production of interleukin-10 ex vivo, upon lipopolysaccharide stimulation. Arthritis Rheum, 2005, 52(5): 1443-1450.
13. Larsson S, Englund M, Struglics A, et al. Interleukin-6 and tumor necrosis factor alpha in synovial fluid are associated with progression of radiographic knee osteoarthritis in subjects with previous meniscectomy. Osteoarthritis Cartilage, 2015, 23(11): 1906-1914.
14. Ma CH, Lv Q, Yu YX, et al. Protective effects of tumor necrosis factor-α blockade by adalimumab on articular cartilage and subchondral bone in a rat model of osteoarthritis. Braz J Med Biol Res, 2015, 48(10): 863-870.
15. Guo H, Luo Q, Zhang J, et al. Comparing different physical factors on serum TNF-α levels, chondrocyte apoptosis, caspase-3 and caspase-8 expression in osteoarthritis of the knee in rabbits. Joint Bone Spine, 2011, 78(6): 604-610.
16. Daheshia M, Yao JQ. The interleukin 1 beta pathway in the pathogenesis of osteoarthritis. J Rheumatol, 2008, 35(12): 2306-2312.
17. Ciombor DM, Aaron RK, Wang S, et al. Modification of osteoarthritis by pulsed electromagnetic field--a morphological study. Osteoarthritis Cartilage, 2003, 11(6): 455-462.
18. Zhao W, Wang T, Luo Q, et al. Cartilage degeneration and excessive subchondral bone formation in spontaneous osteoarthritis involves altered TGF-β signaling. J Orthop Res, 2016, 34(5): 763-770.
19. Zhai GJ, Dore J, Rahman P. TGF-beta signal transduction pathways and osteoarthritis. Rheumatol Int, 2015, 35(8): 1283-1292.
20. Yang CC, Lin CY, Wang HS, et al. Matrix metalloproteases and tissue inhibitors of metalloproteinases in medial plica and pannus-like tissue contribute to knee osteoarthritis progression. PLoS One, 2013, 8(11): e79662.
21. Settle S, Vickery L, Nemirovskiy O, et al. Cartilage degradation biomarkers predict efficacy of a novel, highly selective matrix metalloproteinase 13 inhibitor in a dog model of osteoarthritis: confirmation by multivariate analysis that modulation of type Ⅱ collagen and aggrecan degradation pepti. Arthritis Rheum, 2010, 62(10): 3006-3015.
22. Zamli Z, Adams MA, Tarlton JF. Increased chondrocyte apoptosis is associated with progression of osteoarthritis in spontaneous Guinea pig models of the disease. Int J Mol Sci, 2013, 14(9): 17729-17743.
23. Musumeci G, Castrogiovanni P, Trovato FM, et al. Biomarkers of chondrocyte apoptosis and autophagy in osteoarthritis. Int J Mol Sci, 2015, 16(9): 20560-20575.
24. 谢薇, 周君, 罗庆禄, 等. 脉冲电磁场对兔膝骨关节炎软骨细胞凋亡及凋亡调控蛋白的影响. 四川大学学报: 医学版, 2014(1): 107-110.
25. Mankin HJ, Dorfman H, Lippiello L, et al. Biochemical and metabolic abnormalities in articular cartilage from osteo-arthritic human hips. Ⅱ. Correlation of morphology with biochemical and metabolic data. J Bone Joint Surg Am, 1971, 53(3): 523-537.
26. Pritzker KP, Gay S, Jimenez SA, et al. Osteoarthritis cartilage histopathology: grading and staging. Osteoarthritis Cartilage, 2006, 14(1): 13-29.
27. Carlson CS, Loeser RF, Purser CB, et al. Osteoarthritis in cynomolgus macaques. Ⅲ: Effects of age, gender, and subchondral bone thickness on the severity of disease. J Bone Miner Res, 1996, 11(9): 1209-1217.
28. Pastoureau PC, Hunziker EB, Pelletier JP. Cartilage, bone and synovial histomorphometry in animal models of osteoarthritis. Osteoarthritis Cartilage, 2010, 18(Suppl 3): S106-S112.
29. Laverty S, Girard CA, Williams JM, et al. The OARSI histopathology initiative - recommendations for histological assessments of osteoarthritis in the rabbit. Osteoarthritis Cartilage, 2010, 18(Suppl 3): S53-S65.
30. Gerwin N, Bendele AM, Glasson S, et al. The OARSI histopathology initiative - recommendations for histological assessments of osteoarthritis in the rat. Osteoarthritis Cartilage, 2010, 18(Suppl 3): S24-S34.
31. De Mattei M, Pasello M, Pellati A, et al. Effects of electromagnetic fields on proteoglycan metabolism of bovine articular cartilage explants. Connect Tissue Res, 2003, 44(3/4): 154-159.
32. De Mattei M, Pellati A, Pasello M, et al. Effects of physical stimulation with electromagnetic field and insulin growth factor-Ⅰ treatment on proteoglycan synthesis of bovine articular cartilage. Osteoarthritis Cartilage, 2004, 12(10): 793-800.
33. De Mattei M, Fini M, Setti S, et al. Proteoglycan synthesis in bovine articular cartilage explants exposed to different low-frequency low-energy pulsed electromagnetic fields. Osteoarthritis Cartilage, 2007, 15(2): 163-168.
34. Fini M, Giavaresi G, Torricelli P, et al. Pulsed electromagnetic fields reduce knee osteoarthritic lesion progression in the aged Dunkin Hartley Guinea pig. J Orthop Res, 2005, 23(4): 899-908.
35. Fini M, Torricelli P, Giavaresi G, et al. Effect of pulsed electromagnetic field stimulation on knee cartilage, subchondral and epyphiseal trabecular bone of aged Dunkin Hartley Guinea pigs. Biomed Pharmacother, 2008, 62(10): 709-715.
36. Veronesi F, Torricelli P, Giavaresi G, et al. In vivo effect of two different pulsed electromagnetic field frequencies on osteoarthritis. J Orthop Res, 2014, 32(5): 677-685.
37. Chiba K, Nango N, Kubota S, et al. Relationship between microstructure and degree of mineralization in subchondral bone of osteoarthritis: a synchrotron radiation μCT study. J Bone Miner Res, 2012, 27(7): 1511-1517.
38. Hayami T, Pickarski M, Wesolowski GA, et al. The role of subchondral bone remodeling in osteoarthritis: reduction of cartilage degeneration and prevention of osteophyte formation by alendronate in the rat anterior cruciate ligament transection model. Arthritis Rheum, 2004, 50(4): 1193-1206.
39. Kwan Tat S, Lajeunesse D, Pelletier JP, et al. Targeting subchondral bone for treating osteoarthritis: what is the evidence?. Best Pract Res Clin Rheumatol, 2010, 24(1): 51-70.
40. Castañeda S, Roman-Blas JA, Largo R, et al. Subchondral bone as a key target for osteoarthritis treatment. Biochem Pharmacol, 2012, 83(3): 315-323.
41. Jahns ME, Lou E, Durdle NG, et al. The effect of pulsed electromagnetic fields on chondrocyte morphology. Med Biol Eng Comput, 2007, 45(10): 917-925.
42. Varani K, De Mattei M, Vincenzi F, et al. Characterization of adenosine receptors in bovine chondrocytes and fibroblast-like synoviocytes exposed to low frequency low energy pulsed electromagnetic fields. Osteoarthritis Cartilage, 2008, 16(3): 292-304.
43. Schmidt-Rohlfing B, Silny J, Woodruff S, et al. Effects of pulsed and sinusoid electromagnetic fields on human chondrocytes cultivated in a collagen matrix. Rheumatol Int, 2008, 28(10): 971-977.
44. Chang CH, Loo ST, Liu HL, et al. Can low frequency electromagnetic field help cartilage tissue engineering?. J Biomed Mater Res A, 2010, 92(3): 843-851.
45. Chang SH, Hsiao YW, Lin HY. Low-frequency electromagnetic field exposure accelerates chondrocytic phenotype expression on chitosan substrate. Orthopedics, 2011, 34(1): 20.
46. Sadoghi P, Leithner A, Dorotka R, et al. Effect of pulsed electromagnetic fields on the bioactivity of human osteoarthritic chondrocytes. Orthopedics, 2013, 36(3): e360-e365.

West China Medical Journal

Progress in experimental research on pulsed electromagnetic field in the treatment of knee osteoarthritis

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